American journal of kidney diseases : the official journal of the National Kidney Foundation · 2026
Urinary Metabolites in Tryptophan-Kynurenine Pathway and Risk of CKD Progression in Patients With Type 2 Diabetes.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Liu Jian-Jun, Liu Sylvia, Zheng Huili, Gurung Resham L, Lee Janus, Lee Lye Siang, Ching Jianhong, Ang Keven, Debnath Subrata, Ragi Nagarjunachary, Pyle Laura, Choi Ye Ji, Wu Huijuan, Bjornstad Petter, Sharma Kumar, Lim Su Chi
Аннотация
RATIONALE & OBJECTIVE: Tryptophan-kynurenine pathway is integral for energy metabolism and immune-inflammation regulation. We sought to study the associations between urinary metabolites in tryptophan-kynurenine pathway and risk of chronic kidney disease (CKD) progression in patients with type 2 diabetes.
STUDY DESIGN: Prospective cohort study.
SETTING & PARTICIPANTS: 1,892 participants with type 2 diabetes from Southeast Asia were included in the primary analysis; 951 Chronic Renal Insufficiency Cohort (CRIC) participants with diabetes at baseline were included in the validation study.
EXPOSURES: Urinary tryptophan, kynurenine, 3-hydroxykynurenine, kynurenic acid, xanthurenic acid and kynurenine-to-tryptophan ratio (KTR).
OUTCOMES: CKD progression defined as a composite of incident end stage kidney disease (sustained eGFR < 15 ml/min/1.73m2, maintenance dialysis, renal death) or doubling of serum creatinine concentration.
ANALYTICAL APPROACH: Cause-specific hazard regression.
RESULTS: A total of 224 CKD progression events were identified over a median follow-up of 7.2 years. Each one SD increase in the concentration of urinary kynurenine, 3-hydroxykynurenine, kynurenic acid, and KTR was associated with 1.60 [95% CI 1.16-2.22], 1.64 [1.17-2.31], 1.47 [1.10-1.97] and 1.97 [1.43-2.71] fold higher risk of CKD progression, respectively, after adjustment for known clinical risk factors. These associations were more pronounced in participants with prevalent CKD (eGFR <60 ml/min/1.73m2) compared to those with preserved eGFR. Each one SD increase in urinary tryptophan and kynurenine concentrations was independently associated with 1.60 [1.24-2.06] and 1.35 [1.05-1.73] fold higher risk of CKD progression, respectively, in CRIC participants with diabetes.
LIMITATIONS: Observational study with unmeasured confounding.
CONCLUSIONS: Higher concentrations of urinary metabolites in the tryptophan-kynurenine pathway were associated with higher risk of CKD progression in patients with type 2 diabetes. Future studies are warranted to elucidate the biological mechanisms linking the tryptophan-kynurenine pathway and progression of kidney disease.
STUDY DESIGN: Prospective cohort study.
SETTING & PARTICIPANTS: 1,892 participants with type 2 diabetes from Southeast Asia were included in the primary analysis; 951 Chronic Renal Insufficiency Cohort (CRIC) participants with diabetes at baseline were included in the validation study.
EXPOSURES: Urinary tryptophan, kynurenine, 3-hydroxykynurenine, kynurenic acid, xanthurenic acid and kynurenine-to-tryptophan ratio (KTR).
OUTCOMES: CKD progression defined as a composite of incident end stage kidney disease (sustained eGFR < 15 ml/min/1.73m2, maintenance dialysis, renal death) or doubling of serum creatinine concentration.
ANALYTICAL APPROACH: Cause-specific hazard regression.
RESULTS: A total of 224 CKD progression events were identified over a median follow-up of 7.2 years. Each one SD increase in the concentration of urinary kynurenine, 3-hydroxykynurenine, kynurenic acid, and KTR was associated with 1.60 [95% CI 1.16-2.22], 1.64 [1.17-2.31], 1.47 [1.10-1.97] and 1.97 [1.43-2.71] fold higher risk of CKD progression, respectively, after adjustment for known clinical risk factors. These associations were more pronounced in participants with prevalent CKD (eGFR <60 ml/min/1.73m2) compared to those with preserved eGFR. Each one SD increase in urinary tryptophan and kynurenine concentrations was independently associated with 1.60 [1.24-2.06] and 1.35 [1.05-1.73] fold higher risk of CKD progression, respectively, in CRIC participants with diabetes.
LIMITATIONS: Observational study with unmeasured confounding.
CONCLUSIONS: Higher concentrations of urinary metabolites in the tryptophan-kynurenine pathway were associated with higher risk of CKD progression in patients with type 2 diabetes. Future studies are warranted to elucidate the biological mechanisms linking the tryptophan-kynurenine pathway and progression of kidney disease.